The T wave of an ECG corresponds to

QRS and QT Dispersion and T Wave Abnormalities

Heterogeneity in refractoriness and conduction velocity is a hallmark of reentrant arrhythmias. One index of the heterogeneity of ventricular conduction is derived from the QRS complex duration on surface ECG leads, while heterogeneity of ventricular refractoriness can be found in differences in the length of the QT interval. Dispersion indices usually measure the maximum difference (shortest to longest) in the intervals of interest, which may be adjusted for heart rate and the number of leads sampled (e.g., when the T wave is flat in some leads for QT dispersion). Abnormally high QRS and QT dispersion have been correlated with risk for overall mortality and arrhythmic death in patients with various disorders, although the results are not consistent. Different techniques exist for determining dispersion (including automated algorithms), and the results of one study are often difficult to compare with those of another; in addition, the tests are sensitive to a variety of factors, including age, time of day, season of year, and even body position. More recently, T wave morphology and assessment of the interval from T wave peak to end in lead V5 have been correlated with increased sudden death risk.10 Overall, assessments of these indices have not gained popularity as useful clinical tools. Other details of the QRS complex, such as fragmentation of the conducted complex11 (multiple notches in the QRS;seeFig. 35.4) and the simple width of PVCs,12 have been associated with increased cardiovascular risk.

T Wave

The T wave represents ventricular repolarization. T waves are normally positive, but negative T waves are normal findings in leads aVR and V1 (and in young people, in V2). The causes of pathologic T-wave inversion include myocardial ischemia and infarction, ventricular strain, and treatment with digoxin. Following a myocardial infarction, T-wave inversion develops within 12 to 48 hours and is usually permanent. There is a wide variation in both the duration and the amplitude of the T wave. Flattening T waves are seen with hypokalemia, and peaked T waves are seen with hyperkalemia.

Electrocardiogram During Ventri-cular Repolarization—The t Wave

After the ventricular muscle has become depolarized, about 0.15 second later, repolarization begins and proceeds until complete, at about 0.35 second. This repolarization causes the T wave in the ECG.

Because the septum and endocardial areas of the ventricular muscle depolarize first, it seems logical that these areas should repolarize first as well. However, this is not the usual case, because the septum and other endocardial areas have a longer period of contraction than most of the external surfaces of the heart. Therefore,the greatest portion of ventricular muscle mass to repolarize first is the entire outer surface of the ventricles, especially near the apex of the heart. The endocardial areas, conversely, normally repolarize last. This sequence of repolarization is postulated to be caused by the high blood pressure inside the ventricles during contraction, which greatly reduces coronary blood flow to the endocardium, thereby slowing repolarization in the endocardial areas.

Because the outer apical surfaces of the ventricles repolarize before the inner surfaces, the positive end of the overall ventricular vector during repolarization is toward the apex of the heart.As a result, the normal T wave in all three bipolar limb leads is positive, which is also the polarity of most of the normal QRS complex.

InFigure 12-8, five stages of repolarization of the ventricles are denoted by progressive increase of the light tan areas—the repolarized areas. At each stage, the vector extends from the base of the heart toward the apex until it disappears in the last stage. At first, the vector is relatively small because the area of repolarization is small. Later, the vector becomes stronger because of greater degrees of repolarization. Finally, the vector becomes weaker again because the areas of depolarization still persisting become so slight that the total quantity of current flow decreases. These changes also demonstrate that the vector is greatest when about half the heart is in the polarized state and about half is depolarized.

The changes in the ECGs of the three standard limb leads during repolarization are noted under each of the ventricles, depicting the progressive stages of repolarization. Thus, over about 0.15 second, the period of time required for the entire process to take place, the T wave of the ECG is generated.

Primary T Wave Abnormalities

Primary T wave abnormalities caused by myocardial ischemia or other factors are concordant (i.e., negative T wave in the leads with a dominant S wave or RS pattern) (see Figure 4-8). The significance of concordant T wave changes in the leads with a dominant R wave (i.e., upright T wave) is less certain. In the study by Sgarbossa et al.,64 upright T waves in leads V5 and V6 had a sensitivity of 26 percent for the diagnosis of acute MI, but it is not clear whether this T wave pattern resulted from MI. Upright T waves in the leads with a dominant R wave (i.e., leads I, aVL, V5, V6) are frequently present in subjects with LBBB without MI or other structural myocardial disease. This may occur when the secondary repolarization change caused by LBBB fails to produce T wave inversion but lowers the amplitude of the upright T wave. It may also occur when the location of the transition zone of the QRS complex differs from that of the T wave. This situation can be recognized when the T wave remains upright in leads V5 and V6 but is negative in lead aVL. In many cases, however, the mechanism of a persistent concordant T wave in the leads with an R wave is unexplained by these mechanisms (Figure 4-11).

Abnormalities of the ST Segment and T Wave

A number of drugs and metabolic abnormalities may affect the ST segment and T wave (Fig. 4.7). Hypokalemia may result in prominent U waves in the precordial leads along with prolongation of the QT interval. Hyperkalemia may result in tall, peaked T waves. Hypocalcemia typically lengthens the QT interval, whereas hypercalcemia shortens it. A commonly used cardiac medication, digoxin, often results in diffuse, scooped ST-segment depression. Cardiac pacing, LBBB, and RBBB affect ventricular repolarization and alter the ST segment and T-wave. Minor ornonspecific ST-segment and T-wave abnormalities may occur in many patients and have no definable cause. In these instances, the physician must determine the significance of the abnormalities based on clinical findings.

T Wave

The T wave represents the mid-latter part of ventricular repolarization. A normal T wave has an asymmetrical shape; that is, its peak is closer to the end of the wave than to the beginning (see Fig. 3.6). When the T wave is positive, it normally rises slowly and then abruptly returns to the baseline. When it is negative, it descends slowly and abruptly rises to the baseline. The asymmetry of the normal T wave contrasts with the symmetry of abnormal T waves in certain conditions, such as MI (see Chapters 9 and 10) and a high serum potassium level (see Chapter 11). The exact point at which the ST segment ends and the T wave begins is somewhat arbitrary and usually impossible to pinpoint precisely. However, for clinical purposes accuracy within 40 msec (0.04 sec) is usually acceptable.

LBBB and Ventricular Preexcitation

Transient T wave abnormalities have been observed for variable periods of time after the disappearance of LBBB53 or ventricular preexcitation.54 In patients with preexcitation, T wave abnormalities persisted for days, weeks, and sometimes up to 3 months (see Figure 20-9). The incidence of transient T wave abnormalities and the magnitude of the T wave abnormalities increase with increasing degree of preexcitation (i.e., the duration of the preexcited QRS complex).55,56 No T wave abnormalities occurred in patients with concealed AV bypass conducting only in the retrograde direction. The pattern of primary T wave changes produced by ventricular preexcitation depends on the location of the accessory pathway connections. The septal and posterior connections are associated with more prominent anteriorly directed T wave deflections (i.e., increased amplitude of the T wave in the right and mid-precordial leads) and deviation of the T wave vector superiorly (i.e., negative T waves in leads II, III, and aVF). The left lateral connections are associated with rightward deviation of the T wave in the frontal plane (i.e., T wave inversion or flattening in the left “lateral” leads).57 The distribution of body surface potentials studied before and 1 day and 1 week after ablation of accessory pathways strongly suggests that the transient T wave abnormalities after cessation of preexcitation are caused by AP prolongation over the preexcited area58 and that substantial recovery of action potential duration takes place within 1 week after the ablation.58

The gradual disappearance of primary T wave abnormalities following normalization of intraventricular conduction has been considered a possible manifestation of repolarization “memory.” This implies that the abnormal sequence of activation is “remembered” for some time after return to a normal activa ion pattern.53 Another term applied to describe such a phenomenon is “electrical remodeling.” It is of interest that similar abnormalities have not been recorded in patients with intermittent RBBB.

T Wave Morphology

The T wave is often biphasic or notched. These abnormalities are particularly evident in the precordial leads and contribute to the diagnosis of LQTS; they often are more immediately striking than the sheer prolongation of the QT interval. Following cessation of exercise, major repolarization changes often appear, and they are useful for the diagnosis.

Notched T waves are more frequent in symptomatic patients (81% vs. 19%; p < .005).3 They probably reflect the presence of subthreshold early afterdepolarizations (EADs). Their appearance following exercise is markedly more frequent (85% vs. 3%; p < .0001) among LQTS patients than among healthy controls. Among children, notched T waves are not necessarily abnormal. Gene-specific ECG patterns do exist. LQT1 patients tend to have smooth, broad-based T waves, whereas LQT2 patients frequently have low-amplitude and notched T waves; LQT3 patients have a more distinctive pattern characterized by a late onset of the T wave. However, even within families, extreme heterogeneity of T wave morphology may be observed.

Normal T Wave

Ventricular repolarization—the return of stimulated muscle to the resting state—produces the ST segment, T wave, and U wave. Deciding whether the T wave in any lead is normal is generally straightforward. As a rule, the T wave follows the direction of the main QRS deflection. Thus, when the main QRS deflection is positive (upright), the T wave is normally positive.

Some more specific rules about the direction of the normal T wave can be formulated. The normal T wave is always negative in lead aVR but positive in lead II. Left-sided chest leads such as V4 to V6 normally always show a positive T wave.

The T wave in the other leads may be variable. In the right chest leads (V1 and V2) the T wave may be normally negative, isoelectric, or positive but it is almost always positive by lead V3 in adults. Furthermore, if the T wave is positive in any chest lead, it must remain positive in all chest leads to the left of that lead. Otherwise, it is abnormal. For example, if the T wave is negative in leads V1 and V2 and becomes positive in lead V3, it should normally remain positive in leads V4 to V6.c The differential diagnosis of T wave inversions extending beyond V2 in adults is wide and includes positional and normal variants, right ventricular cardiomyopathy, and acute right ventricular overload syndromes, as well as anterior ischemia.

The polarity of the T wave in the extremity leads depends on the electrical position of the heart. With a horizontal heart the main QRS deflection is positive in leads I and aVL and the T wave is also positive in these leads. With an electrically vertical heart the QRS is positive in leads II, III, and aVF and the T wave is also positive in these leads. However, on some normal ECGs with a vertical axis the T wave may be negative in lead III.

13 T Waves

Inspect the T waves. Normally they are positive in leads with a positive QRS complex. They are also normally positive in leads V3 to V6 in adults, negative in lead aVR, and positive in lead II. The polarity of the T waves in the other extremity leads depends on the QRS electrical axis. (T waves may be normally negative in lead III even in the presence of a vertical QRS axis.) Remember that one of the P waves (with blocked PACs or atrial tachycardia [AT] with block) can “hide” in the T waves, giving it a slightly different appearance from the other T waves.